Electrophilic PPARγ Ligands Attenuate IL-1β and Silica-Induced Inflammatory Mediator Production in Human Lung Fibroblasts via a PPARγ-Independent Mechanism
المؤلفون المشاركون
Phipps, Richard P.
Pollock, Stephen J.
Sime, Patricia J.
Ferguson, Heather E.
Jones, Carolyn
Sapinoro, Ramil E.
Gurell, Michael N.
Thatcher, Thomas H.
Hogan, Christopher M.
المصدر
العدد
المجلد 2011، العدد 2011 (31 ديسمبر/كانون الأول 2011)، ص ص. 1-11، 11ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2011-06-16
دولة النشر
مصر
عدد الصفحات
11
التخصصات الرئيسية
العلوم الطبيعية والحياتية (متداخلة التخصصات)
الأحياء
الملخص EN
Acute and chronic lung inflammation is associated with numerous important disease pathologies including asthma, chronic obstructive pulmonary disease and silicosis.
Lung fibroblasts are a novel and important target of anti-inflammatory therapy, as they orchestrate, respond to, and amplify inflammatory cascades and are the key cell in the pathogenesis of lung fibrosis.
Peroxisome proliferator-activated receptor gamma (PPARγ) ligands are small molecules that induce anti-inflammatory responses in a variety of tissues.
Here, we report for the first time that PPARγ ligands have potent anti-inflammatory effects on human lung fibroblasts.
2-cyano-3, 12-dioxoolean-1, 9-dien-28-oic acid (CDDO) and 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) inhibit production of the inflammatory mediators interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), COX-2, and prostaglandin (PG)E2 in primary human lung fibroblasts stimulated with either IL-1β or silica.
The anti-inflammatory properties of these molecules are not blocked by the PPARγ antagonist GW9662 and thus are largely PPARγ independent.
However, they are dependent on the presence of an electrophilic carbon.
CDDO and 15d-PGJ2, but not rosiglitazone, inhibited NF-κB activity.
These results demonstrate that CDDO and 15d-PGJ2 are potent attenuators of proinflammatory responses in lung fibroblasts and suggest that these molecules should be explored as the basis for novel, targeted anti-inflammatory therapies in the lung and other organs.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Hogan, Christopher M.& Thatcher, Thomas H.& Sapinoro, Ramil E.& Gurell, Michael N.& Ferguson, Heather E.& Pollock, Stephen J.…[et al.]. 2011. Electrophilic PPARγ Ligands Attenuate IL-1β and Silica-Induced Inflammatory Mediator Production in Human Lung Fibroblasts via a PPARγ-Independent Mechanism. PPAR Research،Vol. 2011, no. 2011, pp.1-11.
https://search.emarefa.net/detail/BIM-463069
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Hogan, Christopher M.…[et al.]. Electrophilic PPARγ Ligands Attenuate IL-1β and Silica-Induced Inflammatory Mediator Production in Human Lung Fibroblasts via a PPARγ-Independent Mechanism. PPAR Research No. 2011 (2011), pp.1-11.
https://search.emarefa.net/detail/BIM-463069
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Hogan, Christopher M.& Thatcher, Thomas H.& Sapinoro, Ramil E.& Gurell, Michael N.& Ferguson, Heather E.& Pollock, Stephen J.…[et al.]. Electrophilic PPARγ Ligands Attenuate IL-1β and Silica-Induced Inflammatory Mediator Production in Human Lung Fibroblasts via a PPARγ-Independent Mechanism. PPAR Research. 2011. Vol. 2011, no. 2011, pp.1-11.
https://search.emarefa.net/detail/BIM-463069
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-463069
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
تقوم هذه الخدمة بالتحقق من التشابه أو الانتحال في الأبحاث والمقالات العلمية والأطروحات الجامعية والكتب والأبحاث باللغة العربية، وتحديد درجة التشابه أو أصالة الأعمال البحثية وحماية ملكيتها الفكرية. تعرف اكثر